(MENAFN) Researchers at the Children’s Hospital of Philadelphia (CHOP) have uncovered multiple genetic factors tied to reduced bone density in children and adolescents, potentially paving the way for earlier interventions and stronger lifelong bone health.

In a study published in Genome Biology, scientists analyzed genetic markers previously associated with bone mineral density in large-scale genome-wide association studies, media reported Wednesday.

Employing CRISPRi, a gene-suppressing technology that does not cut DNA, the team pinpointed four genes—ARID5B, CC2D1B, EIF4G2, and NCOA3—that play a key role in osteoblast maturation. Osteoblasts are specialized cells responsible for building new bone, a process that is most active during childhood and adolescence.

The research also revealed that many bone-related genetic signals may impact other tissues, indicating broader health implications for children.

“With this information, our hope is to further study these signals specifically in pediatrics and help identify which children are more likely to get a fracture to optimize their bone health for life,” said senior study author Struan F.A. Grant.

In a separate study published in the Journal of Bone and Mineral Research, scientists examined the predictive power of a polygenic risk score called gSOS, previously used to forecast fracture risk in adults.

Drawing on long-term data from the Bone Mineral Density in Childhood Study and CHOP’s Center for Applied Genomics, researchers found that higher gSOS scores were linked to stronger bone density at multiple skeletal sites and a lower fracture risk—even after accounting for diet, puberty, body size, and prior injuries.

The studies underscore the substantial role genetics play in bone strength throughout life and suggest a future where clinicians could identify children at high fracture risk and implement early interventions alongside tailored diet and weight-bearing exercise.

MENAFN20112025000045017169ID1110373724